title: Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure.
abstract: BACKGROUND
  Chronic heart failure (CHF) is associated with endothelial dysfunction including impaired endothelium-mediated, flow-dependent dilation (FDD). There is evidence for increased radical formation in CHF, raising the possibility that nitric oxide is inactivated by radicals, thereby impairing endothelial function. To test this hypothesis, we determined the effect of the antioxidant vitamin C on FDD in patients with CHF.
  
  
  RESULTS
  High-resolution ultrasound and Doppler was used to measure radial artery diameter and blood flow in 15 patients with CHF and 8 healthy volunteers. Vascular effects of vitamin C (25 mg/min IA) and placebo were determined at rest and during reactive hyperemia (causing endothelium-mediated dilation) before and after intra-arterial infusion of N-monomethyl-L-arginine (L-NMMA) to inhibit endothelial synthesis of nitric oxide. Vitamin C restored FDD in patients with heart failure after acute intra-arterial administration (13.2+/-1.7% versus 8.2+/-1.0%; P<.01) and after 4 weeks of oral therapy (11.9+/-0.9% versus 8.2+/-1.0%; P<.05). In particular, the portion of FDD mediated by nitric oxide (ie, inhibited by L-NMMA) was increased after acute as well as after chronic treatment (CHF baseline: 4.2+/-0.7%; acute: 9.1+/-1.3%; chronic: 7.3+/-1.2%; normal subjects: 8.9+/-0.8%; P<.01).
  
  
  CONCLUSIONS
  Vitamin C improves FDD in patients with CHF as the result of increased availability of nitric oxide. This observation supports the concept that endothelial dysfunction in patients with CHF is, at least in part, due to accelerated degradation of nitric oxide by radicals.
authors.affiliation: Abteilung Kardiologie, Medizinische Hochschule Hannover, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Hornig
authors.forename: N
authors.initials: N
authors.lastname: Arakawa
authors.forename: C
authors.initials: C
authors.lastname: Kohler
authors.forename: H
authors.initials: H
authors.lastname: Drexler
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D002303:Cardiac Output, Low / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007269:Injections, Intra-Arterial; D008297:Male; D008875:Middle Aged; D017534:Radial Artery / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D016896:Treatment Outcome; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D001205:Ascorbic Acid